I'm surprised that there's not been a Synaptic thread. If I had to sell everything in my portfolio, SNAP might be the last holding to go. It's for the patient investor, however.
This is another company that John De Castro pointed out for me. SNAP, to me, is one of those companies where, as one component of a basket of similar companies, you can close your eyes for five years and wake up rich. There should be another partnership (to complement those with Ciba-Geigy/Novartis, Lilly and Merck) announced soon. Here's an interesting abstract.......
Medline ID:
96177284
Citation:
Schwartz MW, Baskin DG, Bukowski TR, Kuijper JL,
Foster D,
Lasser G, Prunkard DE, Porte D Jr, Woods SC, Seeley
RJ,
Weigle DS, Specificity of leptin action on elevated
blood
glucose levels and hypothalamic neuropeptide Y gene
expression in ob/ob mice., Diabetes 45: 4, 531-5,
Apr, 1996.
Abstract
Correction of the obese state induced by genetic leptin deficiency
reduces elevated levels
of both blood glucose and hypothalamic neuropeptide Y (NPY) mRNA in
ob/ob mice. To
determine whether these responses are due to a specific action of
leptin or to the reversal
of the obese state, we investigated the specificity of the effect of
systemic leptin
administration to ob/ob mice (n = 8) on levels of plasma glucose and
insulin and on
hypothalamic expression of NPY mRNA. Saline-treated controls were
either fed ad
libitum (n = 8) or pair-fed to the intake of the leptin-treated group
(n = 8) to control for
changes of food intake induced by leptin. The specificity of the
effect of leptin was
further assessed by 1) measuring NPY gene expression in db/db mice (n
= 6) that are
resistant to leptin, 2) measuring NPY gene expression in brain areas
outside the
hypothalamus, and 3) measuring the effect of leptin administration on
hypothalamic
expression of corticotropin-releasing hormone (CRH) mRNA. Five daily
intraperitoneal
injections of recombinant mouse leptin (150 micrograms) in ob/ob mice
lowered food
intake by 56% (P < 0.05), body weight by 4.1% (P < 0.05), and levels
of NPY mRNA in
the hypothalamic arcuate nucleus by 42.3% (P < 0.05) as compared with
saline-treated
controls. Pair-feeding of ob/ob mice to the intake of leptin-treated
animals produced
equivalent weight loss, but did not alter expression of NPY mRNA in
the arcuate nucleus.
Leptin administration was also without effect on food intake, body
weight, or NPY
mRNA levels in the arcuate nucleus of db/db mice. In ob/ob mice,
leptin did not alter
NPY mRNA levels in cerebral cortex or hippocampus or the expression
of CRH mRNA
in the hypothalamic paraventricular nucleus (PVN). Leptin
administration to ob/ob mice
also markedly reduced serum glucose (8.3 +/- 1.2 vs. 24.5 +/- 3.8
mmol/l; P < 0.01) and
insulin levels (7,263 +/- 1,309 vs. 3,150 +/- 780 pmol/l), but was
ineffective in db/db
mice. Pair-fed mice experienced reductions of glucose and insulin
levels that were < 60%
of the reduction induced by leptin. The results suggest that in ob/ob
mice, systemic
administration of leptin inhibits NPY gene overexpression through a
specific action in the
arcuate nucleus and exerts a hypoglycemic action that is partly
independent of its
weight-reducing effects. Furthermore, both effects occur before
reversal of the obesity
syndrome. Defective leptin signaling due to either leptin deficiency
(in ob/ob mice) or
leptin resistance (in db/db mice) therefore leads directly to
hyperglycemia and the
overexpression of hypothalamic NPY that is implicated in the
pathogenesis of the obesity
syndrome.
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Disclaimer: I own shares of SNAP, and I have a vested interest in their appreciation. I am not qualified to make recommendations. Do your own homework.
Cheers! Rick |
